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Get ahead!
medicine
300 SBAs for finals
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Get ahead!
medicine
300 SBAs for finals
Series Editor:
Saran Shantikumar MD Academic Clinical
Fellow in Surgery, Nuffield Department of
Surgery, John Radcliffe Hospital, Oxford, UK
Authors:
Benjamin McNeillis BA BM BCH F2 DOCTOR, Oxford
Deanery, John Radcliffe Hospital, Oxford, UK
Rhian James MA (HONS) BM BCHIR F2 DOCTOR,
Heatherwood and Wexham Park Hospital Trust,
Slough, UK
Ai Ling Koh MB CHB F2 DOCTOR, Oxford Deanery,
Wexham Park Hospital, Slough, UK
Tim Sparkes MBBS BENG F2 DOCTOR, Oxford
Deanery, John Radcliffe Hospital, Oxford, UK
First published in Great Britain in 2012 by
Hodder Arnold, an imprint of Hodder Education, a division of Hachette UK
338 Euston Road, London NW1 3BH
http://www.hodderarnold.com
© 2012 Hodder & Stoughton Ltd
All rights reserved. Apart from any use permitted under UK copyright law, this publication may only be
reproduced, stored or transmitted, in any form, or by any means with prior permission in writing of the
publishers or in the case of reprographic production in accordance with the terms of licences issued by the
Copyright Licensing Agency. In the United Kingdom such licences are issued by the Copyright Licensing
Agency: Saffron House, 6–10 Kirby Street, London EC1N 8TS.
Hachette UK’s policy is to use papers that are natural, renewable and recyclable products and made from
wood grown in sustainable forests. The logging and manufacturing processes are expected to conform to the
environmental regulations of the country of origin.
Whilst the advice and information in this book are believed to be true and accurate at the date of going to
press, neither the author[s] nor the publisher can accept any legal responsibility or liability for any errors or
omissions that may be made. In particular, (but without limiting the generality of the preceding disclaimer)
every effort has been made to check drug dosages; however it is still possible that errors have been missed.
Furthermore, dosage schedules are constantly being revised and new side-effects recognized. For these reasons
the reader is strongly urged to consult the drug companies’ printed instructions, and their websites, before
administering any of the drugs recommended in this book.
British Library Cataloguing in Publication Data

A catalogue record for this book is available from the British Library
Library of Congress Cataloging-in-Publication Data

A catalog record for this book is available from the Library of Congress
ISBN-13 978-1-853-15732-5
1 2 3 4 5 6 7 8 9 10
Commissioning Editor: Sarah Penny

Project Management: Naughton Project Management Ltd
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Printed and bound in the UK by CPI Anthony Rowe
What do you think about this book? Or any other Hodder Arnold title?
Please visit our website: www.hodderarnold.com
Contents
Contents
Contents v
Preface viii
Introduction to Get Ahead Medicine xiv
Practice Practice Paper 1: Questions 1

1. Acute coronary syndrome (1) 1
2. Obstructive renal impairment 1
3. Management of skin lesions (1) 1
4. Chest X-ray 2
5. Headaches 2
6. Chronic obstructive pulmonary disease 2
7. Management of asthma (1) 2
8. Collapse (1) 3
9. Eczema versus psoriasis 3
10. Diagnosis of multiple sclerosis (1) 3
11. The multidisciplinary team 4
12. Diagnosis of chest pain (1) 4
13. Risk factors for ischaemic heart disease 4
14. Diagnosis of cough (1) 4
15. Diagnosis of vertigo 5
16. Epistaxis 5
17. Diarrhoea (1) 6
18. Diagnosis of malaria 6
19. Electrocardiogram (1) 6
20. Investigation of deranged liver function tests 6
21. Epigastric pain (1) 7
22. Gout prophylaxis 7
23. Hepatomegaly 7
24. Sclerosing cholangitis 8
25. Investigation of status epilepticus 8
26. Shortness of breath (1) 8
27. Aortic regurgitation 8
28. Management of oliguria (1) 9
29. Steatorrhoea 9
30. Management of Parkinson’s disease (1) 10
31. Autoantibodies 10
32. Coronary circulation 10
33. Management of anaemia 10
34. ACE inhibitors 11 v
35. Microbiology 11
Contents
36. Skin lesions (1) 11
37. Diagnosis of abdominal pain (1) 11
38. Ankylosing spondylitis 12
39. Mitral stenosis 12
40. Management of facial weakness 12
41. Pathological fracture 12
42. Management of HIV 13
43. Tetralogy of Fallot 13
44. Investigation of dysphagia 13
45. Thalassaemia trait 14
46. Warfarin therapy 14
47. The painful joint 14
48. The unresponsive patient (1) 15
49. Vomiting 15
50. Weight loss 15
Practice Paper 1: Answers 16
Practice Paper 2: Questions 40

1. Acute confusion 40
2. HLA-B27 40
3. Heart failure (1) 40
4. Scoring systems (1) 40
5. Investigation of headache (1) 41
6. Management of hypercalcaemia 41
8. Nosebleeds 42
9. Haematemesis 42
10. Failure to thrive 43
11. Osteoarthritis of the hand 43
12. Study design 43
14. Mouth ulcers 44
15. Antibiotics (1) 44
16. Pleural effusion 44
17. Topical steroids 45
18. Skin lesion (2) 45
19. Management of Parkinson’s disease (2) 45
20. Arrhythmias 46
21. Back pain 46
22. Bruising in children 46
24. Coarctation of the aorta 47
vi
25. Management of asthma (2) 47
26. Collapse (2) 48
Contents
28. Investigation of stroke 48
30. Diagnosis of multiple sclerosis (2) 49
31. Investigation of abdominal pain 49
33. Diagnosis of tuberculosis 50
34. Thrombocytopenia 50
35. Meningitis 51
37. Diarrhoea (2) 51
38. Management of epilepsy 52
39. Diagnosis of HIV-related illness 52
40. Tiredness 52
41. Management of acne (1) 53
42. Epigastric pain (2) 53
43. Sexually transmitted infections (1) 53
44. Non-steroidal anti-inflammatories 54
45. Renal transplantation 54
46. Thrombolysis in ischaemic stroke 54
48. Management of oliguria (2) 55
49. The unresponsive patient (2) 55
50. Thyrotoxicosis 56

2. Haematuria 82
3. Heart failure (2) 83
4. Hodgkin’s lymphoma 83
5. Management of psoriasis 83
6. Subarachnoid haemorrhage 84
7. Overdose and antidotes (1) 84
8. Pneumonia 84
9. Murmur (1) 84
10. Skin lesions (3) 85
11. Antibiotics (2) 85
13. Investigation of headache (2) 86
14. Management of hyperglycaemia (1) 86
vii
16. Fatigue 87
17. Arterial blood gases (1) 87
Contents
19. Management of chest pain (1) 88
20. Barium enema 88
21. Cardiovascular examination 89
22. Cauda equina syndrome 89
23. Joint swelling 89
24. Coeliac disease 90
25. Complications of alcoholic liver disease 90
27. Disseminated intravascular coagulation 90
28. Rectal bleeding (1) 91
30. Diagnosis of gout 91
31. Investigation of shortness of breath (1) 92
32. Diagnosis of neurological dysfunction (1) 92
33. Management of multiple sclerosis 93
34. Diagnosis of stroke 93
36. Management of diarrhoea 94
38. Endocarditis 94
40. Ingested foreign body 95
41. Management of acne (2) 95
42. Statistics (1) 96
44. Management of shortness of breath (1) 96
45. Signs of liver disease (1) 97
46. Non-invasive ventilation 97
47. Systemic lupus erythematosus (1) 97
48. Medications in hyperkalaemia 98
49. Tumour markers 98
50. Parkinson’s disease 98

1. Airway management 124
2. Management of pulmonary embolism 124
3. Skin manifestations of systemic disease (1) 124
6. Investigation of hepatomegaly 125
viii
7. Substance use (1) 126
8. Home oxygen 126
Contents
9. Management of chest pain (2) 126
10. Antibiotics in pregnancy 127
11. Left ventricular hypertrophy 127
13. Polycystic kidney disease (1) 128
14. Management of status epilepticus 128
15. Overdose and antidotes (2) 128
16. Murmur (2) 129
18. Helicobacter pylori infection 129
20. Drug administration 130
22. Fluid therapy 131
23. Haemolytic anaemia 131
24. Basic life support 132
25. Causes of tremor 132
26. Biological therapies 132
27. Cognitive impairment (1) 133
28. Complications of blood transfusion 133
29. Diagnosis of numbness 133
30. Diagnosis of postural hypotension 134
31. Management of delirium 134
32. Liver function tests 134
34. Diagnosis of skin lesions (1) 135
37. Management of ischaemic stroke 136
38. Malignant melanoma (1) 137
39. Nipple discharge 137
40. Palpitations (1) 137
41. Diagnosis of endocrine disease 138
42. Emollient use 138
43. Medications in acute renal failure 138
44. Rectal bleeding (2) 138
45. Signs of liver disease (2) 139
46. Indications for haemodialysis in acute renal failure 139
49. Uraemia 140
50. Urinary frequency (1) 140
ix
Contents
1. Alzheimer’s disease 164

2. Antibiotics with warfarin 164
4. Secondary prevention 165
5. Investigation of hypothyroidism 165
6. Sickle cell disease 165
7. Substance use (2) 166
8. Skin manifestations of systemic disease (2) 166
9. Hepatic haemangioma 166
10. Oxygen therapy 167
11. Polycystic kidney disease (2) 167
12. Myalgia 167
13. Hyperbilirubinaemia 168
14. Drugs used in cardiac arrest 168
15. Management of thyrotoxicosis 168
16. Haemoptysis (1) 168
18. Dry eyes 169
20. Management of decreased consciousness 170
21. Haemophilia 170
22. Gastrointestinal pathology 170
23. Blood film 170
24. Lung cancer 171
25. Cavernous sinus lesions 171
26. Cognitive impairment (2) 172
27. Complications of bone marrow transplant 172
33. Malignant melanoma (2) 174
35. Diagnosis of chest infection (1) 175
36. Emergency management (1) 175
37. Investigation of shortness of breath (2) 176
39. Hypoxia 176
40. Management of hypothermia 177
41. Diagnosis of diabetes 177
42. Medication review 177
43. Side effects of methotrexate 178
x
44. Raised intracranial pressure 178
Contents
45. Bronchial carcinoma 178
46. Neurological dysfunction 179
47. Diagnosis of rheumatoid arthritis (1) 179
48. Statistics (2) 179
49. Sepsis syndromes 180
50. Nephrotic syndrome 180

1. Amenorrhoea 203
2. Myasthenia gravis 203
3. Hyperkalaemia 203
4. Myocardial infarction 204
5. Pruritus 204
6. Seizures 204
7. Spinal cord compression 204
8. Sepsis 205
9. Radiographic changes in ankylosing spondylitis 205
10. Management of toxicity 205
11. Squamous cell carcinoma 206
12. Management of urinary tract infection 206
13. Side effects of anti-tuberculous medication 206
14. Hypothyroidism 206
15. Painful fingers 207
17. Haemoptysis (2) 207
18. Antibody testing 208
20. Atrial fibrillation 208
21. Blood groups 208
22. Generalised weakness 209
23. Investigation of jaundice 209
24. Management of skin conditions 209
25. Investigation of muscle weakness 210
26. Hepatitis serology 210
27. Lumbar puncture 210
28. Management of hyperkalaemia 211
29. Management of hypertension 211
30. Malabsorption 211
31. Brain tumours 212
32. Chest injury 212
33. Complications of hepatitis infection 212
xi
34. Conn’s syndrome 213
35. Dysphagia 213
Contents
36. Diagnosis of chest infection (2) 213
38. Diagnosis of Cushing’s syndrome 214
40. Diagnosis of rheumatoid arthritis (2) 215
43. Emergency management (2) 216
44. Supraventricular tachycardia 216
45. Syndrome of inappropriate ADH secretion 216
47. Urinary frequency (2) 217
48. Wilson’s disease 218
49. X-ray changes in osteoarthritis 218
50. Traveller’s diarrhoea 218
Index of topics covered 243
xii
Preface
Preface
Welcome to Get ahead! Medicine. This book contains 300 Single Best Answer
(SBA) questions covering various topics within clinical surgery. The SBAs
are arranged as six practice papers, each containing 50 questions. Allow
yourself 60–90 minutes for each paper. You can either work through the
practice papers systematically or dip in and out of the book using the SBA
index as a guide to where questions on a specific topic can be found. We have
tried to include all the main conditions about which you can be expected
to know, as well as some more detailed knowledge suitable for candidates
aiming towards distinction. As in the real exam, these papers have no preset
pass mark. Whether you pass or fail depends on the distribution of scores
across the whole year group, but around 60% should be sufficient.
We hope this book fulfils its aim in being a useful, informative revision
aid. If you have any feedback or suggestions, please let us know
([email protected]).
We would like to acknowledge the help of Sarah Vasey, Jo Koster and
Sarah Penny of Hodder Arnold, for their guidance, support and patience
throughout this project.
Ben McNeillis
Rhian James
Ai Ling Koh
Tim Sparkes
Saran Shantikumar
xiii
Introduction to Get Ahead Medicine
GET AHEAD!
Single Best Answer questions (SBAs) are becoming more popular as a
method of assessment in summative medical school examinations. Each
clinical vignette is followed by a list of five possible answers, of which only
one is correct. SBAs have the advantage of testing candidates’ knowledge of
clinical scenarios rather than their ability at detailed factual recall. They do
not always parallel real-life situations, however, and are no comparison to
clinical decision making. Either way the SBA is here to stay.
The Get ahead! series is aimed primarily at undergraduate finalists. Much
like the real exam we have endeavoured to include commonly asked
questions as well as a generous proportion of harder stems, appropriate for
the more ambitious student aiming for honours. The Universities Medical
Assessment Partnership (UMAP) is a collaboration of 14 medical schools
in the UK, which is compiling a bank of SBAs and EMQs to be used in
summative examinations. The questions in the Get ahead! series are written
to closely follow the ‘house style’ of the UMAP SBAs, and hence are of
a similar format to what many of you can expect in your exams. All the
questions in the Get ahead! series are accompanied by explanatory answers
including a succinct summary of the key features of each condition. Even
when you get an answer right I strongly suggest you read these – I guarantee
you’ll learn something. For added interest we have included details of
eponymous persons (‘eponymous’ from Greek epi = upon + onyma = name;
‘giving name’) and, as you have just seen, some derivations of words from
the original Latin or Greek.
HOW TO PASS YOUR EXAMS

The clinical scenarios given in SBAs are intended to be based on ‘house
officer knowledge’. Sadly this is not always the case and you shouldn’t be
surprised when you get a question concerning the underlying histology
of testicular tumours (as I was). So start revising early and don’t restrict
yourself to the given syllabus if you can avoid it. If your exam is only 2 weeks
away then CRAM, CRAM, CRAM – you’ll be surprised at how much you
can learn in a fortnight.
DURING THE EXAM

1. Try to answer the questions without looking at the responses at first – the
questions are written such that this should be possible.
2. Take your time to read the questions fully. There are no bonus marks
xiv available for finishing the paper early.
3. If you get stuck on a question then make sure you mark down your best

guess before you move on. You may not have time to come back to it at
the end.
4. Answer all the questions – there is no negative marking. If you are unsure
go with your instinct – it’s probably going to be your best guess.
5. Never think that the examiner is trying to catch you out. Red herrings
are not allowed so don’t assume there is one. If a question looks easy it
probably is!
This is obvious: there is no substitute for learning the material thoroughly
and practising as many questions as you can. With this book you’re off to a
good start!
A FINAL WORD
The Get ahead! series is written by junior doctors who have recently finished
finals and who have experience teaching students. As such, I hope the books
cover information that is valuable and relevant to you as undergraduates
who are about to sit finals.
I wish you the best of luck in your exams!
Saran Shantikumar
Series editor, Get ahead!
xv
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Practice Paper 1: Questions
1. Acute coronary syndrome (1)
In the treatment of acute coronary syndrome (ACS), which of the following
statements is FALSE?
A Aspirin and clopidogrel do not provide enough anticoagulation; heparin
should also be given
B Give 75 mg aspirin stat
C Give 300 mg clopidogrel in addition to aspirin
D Hypotension, asthma and bradycardia are the main contraindicators to
beta blockade
E Patients will likely continue taking a statin, beta-blocker and angiotensin-
converting enzyme (ACE) inhibitor on discharge home
2. Obstructive renal impairment

Which of the following is not a potential cause of obstructive renal
impairment?
A Benign prostatic hypertrophy
B Recurrent kidney stones
C Retroperitoneal fibrosis
D Schistosomiasis
E Systemic sclerosis
3. Management of skin lesions (1)

A 60-year-old man who works for an oil company presents with a lesion
on the temple that is bothering him as it is growing. It bled once when he
knocked it. On examination, the lesion is 8 mm in diameter and is a flat,
mildly erythematous patch with a few scales and a larger keratotic horn
in the centre. There are no other lesions on inspection of his skin and no
personal or family history of skin cancer.
Which of the following is the most appropriate management plan?
A Cryotherapy
B Curettage
C Excisional biopsy
D Topical 5-fluorouracil
E Wide local excision
1
4. Chest X-ray
A 68-year-old man who is recently diagnosed with lung cancer is admitted

to the emergency department with acute shortness of breath. A chest X-ray
shows a right upper zone (RUZ) collapse.
What do you expect to find on examination?
Trachea Percussion Auscultation
A Deviated to right Dull RUZ Reduced breath sounds
B Deviated to right Dull RUZ Wheeze
C Deviated to right Resonant RUZ Reduced breath sounds
D Deviated to left Dull RUZ Reduced breath sounds
E Deviated to left Resonant RUZ Wheeze
5. Headaches
A 68-year-old woman presents to her GP with headaches and visual
disturbance. She has also noticed that she gets an itchy rash when she
gets out of a hot bath. On examination she has a ruddy complexion and
a palpable spleen. Her only previous medical history is gout. Initial blood
tests reveal a raised packed red cell volume with a raised red cell mass, along
with a raised white cell count and thrombocytosis.
What is the most likely diagnosis?
A Chronic myeloid leukaemia
B Lymphoma
C Migraine with aura
D Polycythaemia rubra vera
E Soap allergy
6. Chronic obstructive pulmonary disease

A 45-year-old man who is a heavy smoker is recently diagnosed with
chronic obstructive pulmonary disease (COPD). He has no documented
acute exacerbations in the past.
Which of the following treatment is NOT suitable in the management of
COPD in this patient?
A Annual influenza and pneumococcal vaccination
B Inhaled corticosteroids
C Short-acting b2-agonist
D Short-acting anti-cholinergic
E Smoking cessation
7. Management of asthma (1)

A 35-year-old woman is admitted to hospital with quick-onset shortness of
breath. She has a past medical history of asthma. Her observations include
2
a pulse rate 120 bpm, blood pressure 100/72 mmHg, respiratory rate 30/
min and SaO2 88% on room air. On examination, she appears to be drowsy

and exhausted. Her chest is quiet on auscultation. Arterial blood gases
show: pH 7.35, PaO2 5.2 kPa, PaCO2 4.9 kPa and bicarbonate 24 mmol/L.
Which of the following would NOT be appropriate in the management of
this case?
A High-flow oxygen
B High-dose nebulised beta-2 agonists
C Intravenous magnesium sulphate
D Leukotriene receptor antagonists
E Steroids
8. Collapse (1)
A 19-year-old footballer has collapsed on the pitch. His airway is clear and
he is brought to the emergency department, where he begins to recover and
denies that he has chest pain. He has never had anything like this before.
Which of the following is the most likely diagnosis?
A Carotid stenosis
B Hypertrophic obstructive cardiomyopathy (HOCM)
C Myocardial infarction
D Rheumatic fever
E Thyrotoxicosis
9. Eczema versus psoriasis

A 31-year-old man presents to your clinic with a year-long history of itchy
red scaly lesions.
Which of the following would make you more likely to diagnose eczema
rather than psoriasis?
A Associated nail changes
B History of distal interphalangeal joint pain and swelling
C Localised to flexures rather than extensors
D Well-demarcated lesions
E Worsening in winter months
10. Diagnosis of multiple sclerosis (1)

Which of the following best describes the MRI findings in multiple sclerosis?
A Cortical grey matter inflammatory lesions
B Longitudinally extensive transverse myelitis (more than three spinal
segments)
C Periventricular white matter lesions matching the clinical picture
D Periventricular white matter lesions not necessarily matching the clinical
picture
E White matter lesions exclusively in the cerebellum and brainstem 3
11. The multidisciplinary team
A 67-year-old man is discharged from hospital following an incision and

drainage of a large abdominal wall abscess. He needs someone to help
change his wound packing regularly, however he is immobile and lives
alone.
Which member of the multidisciplinary team would be most appropriate
to help?
A District nurse
B Health visitor
C Occupational therapist
D Orthotist
E Social worker
12. Diagnosis of chest pain (1)

A 69-year-old man presents to the emergency department with ongoing
chest pain. He has a past medical history of intermittent claudication and
hypertension. He is an overweight smoker and heavy drinker of alcohol.
On analysing the electrocardiogram (ECG), you notice broad S-waves in
the right-hand chest leads, two R-waves per complex in the left-hand chest
leads and ST-segment elevation. He asks if he has had a heart attack.
What is the best answer to this question?
A No – but we need to do more tests to find the true cause
B No – it’s just right bundle branch block
C No – it’s just angina
D Yes
E I’m not sure; we need to do more tests
13. Risk factors for ischaemic heart disease

Which of the following is not a preventable risk factor for coronary artery
disease?
A Five cigarettes per day smoking history
B High low-density lipoprotein (LDL) cholesterol levels
C Hypertension
D Obesity
E 12 U/week alcohol history
14. Diagnosis of cough (1)

A 29-year-old man presents to the emergency department with a 1-week
history of non-productive cough, muscle aches, fever, vomiting and
diarrhoea. His observations include temperature 38.4°C, pulse rate 105
4
bpm, blood pressure 110/76 mmHg and respiratory rate 22/min. On
examination, his chest is clear to both auscultation and percussion. A chest

X-ray shows bilateral lung basal infiltrates. The blood results show Na+ 128
mmol/L, K+ 4.0 mmol/L, urea 5.9 mmol/L, creatinine 130 mmol/L, albumin
26 g/L, ALT 106 IU/L, ALP 230 IU/L.
What is the most likely causative organism?
A Chlamydia pneumoniae
B Mycoplasma pneumoniae
C Legionella pneumophila
D Staphylococcus aureus
E Streptococcus pneumoniae
15. Diagnosis of vertigo

A 60-year-old man presents with a history of recurrent dizzy spells for the
past 4 months, which occur daily. The dizzy spells last a few minutes and
seem to occur if he moves his head, as a result of which he keeps his head as
still as possible. The attacks are not associated with any deafness or tinnitus
and a neurological examination is entirely normal. You favour a diagnosis
of benign paroxysmal positional vertigo.
Which of the following descriptions of findings on Hallpike’s manoeuvre
would confirm this diagnosis?
A Delayed onset (a few seconds) torsional nystagmus on descent facing
both sides
B Delayed onset (a few seconds) torsional nystagmus on descent facing one
side only
C Immediate torsional nystagmus on descent facing both sides
D Immediate torsional nystagmus on descent facing one side only
E No nystagmus on descent facing either side
16. Epistaxis
A 43-year-old man presents to his GP with a 3-month history of recurrent
nose bleeds, mucosal bleeding, haemoptysis and recurrent sinusitis. Besides
that, he also noticed that he has increasingly become short of breath. On
examination, he had a nasal deformity and chest auscultation revealed
crackles in the left lower zone. A urine dipstick test showed microscopic
haematuria.
A Chronic myeloid leukaemia
B Chronic lymphocytic leukaemia
C Churg–Strauss syndrome
D Goodpasture syndrome
5
E Wegener granulomatosis
17. Diarrhoea (1)
Following a protracted stay in hospital following a severe chest infection,

an 83-year-old man develops bloody diarrhoea.
What is the most likely cause?
A Adenocarcinoma of the bowel
B Clostridium difficile infection
C Norovirus infection
D Salmonella infection
E Shigella infection
18. Diagnosis of malaria

A 21-year-old student on an internship with The Guardian travel section
has recently returned from a backpacking holiday in West Africa. For the
last few days he has been having headaches, flu-like symptoms and muscle
aches, and now he has started rigoring.
Which investigation should be performed to rule out malaria?
A Blood cultures
B Falciparum antigen dipstick test
C Liver biopsy
D One blood film
E Three thick and thin blood films on consecutive days
19. Electrocardiogram (1)

You are asked to review an electrocardiogram (ECG) in the emergency
department. Helpfully, a summary of details is printed at the top as follows:
rate 88/min, regular rhythm, axis –20°, PR duration 0.26 seconds (constant),
QRS complex 0.08 seconds, QT interval 0.2 seconds. You note that P-waves
are only present before each QRS and that the rhythm is regular.
Which of the following would be the best summary?
A First-degree heart block
B Left axis deviation
C Left bundle branch block
D Refuse to summarise until it can be compared with an old ECG
E Ventricular tachycardia
20. Investigation of deranged liver function tests

A 65-year-old man with a longstanding diagnosis of chronic obstructive
pulmonary disease has been reviewed by his GP for deteriorating liver
function tests and clinical signs and symptoms of cirrhosis.
6
What investigation should the GP arrange?
A Alpha-1-antitrypsin serum levels

B Alpha-feto protein levels
C Anti-smooth muscle antibodies
D Gamma GT levels
E Hepatitis screen
21. Epigastric pain (1)

A 44-year-old woman presents to the emergency department with pain.
The pain is epigastric, sharp in nature, worse on lying flat and during
inspiration. She has recently suffered a chest infection. She is not a smoker.
On examination, she has diffuse inspiratory crepitations. Her oxygen
saturation is 98% on room air. Her ECG shows widespread saddle-shaped
ST elevation.
A Acute pericarditis
B Angina
C Myocardial infarction
D Pleurisy
E Pulmonary embolism
22. Gout prophylaxis

A 55-year-old overweight pub landlord presents with a several-year history
of episodic acute painful joint swelling that started in his left big toe and
now affects his knees. Symptoms improve with use of diclofenac. Gout was
diagnosed on his first hospital visit, however this now appears recurrent.
He developed an acute attack in his left knee 2 days ago.
Which of the following represents the best plan for prophylaxis?
A Keep on long-term diclofenac with gastric protection
B Start allopurinol now with non-steroidal anti-inflammatory drugs
(NSAIDs) cover and increase until his urate is below 300 mmol/L
C Start allopurinol at least 2 weeks after the acute attack has settled with
NSAID cover and increase until his urate level is below 300 mmol/L
D Switch to long-term colchicine
E Switch to use of depot steroid injections
23. Hepatomegaly
Which of the following conditions does not classically cause hepatomegaly?
A End-stage cirrhosis
B Fatty liver
C Hepatocellular carcinoma
D Myeloproliferative disease
7
E Right-sided heart failure
24. Sclerosing cholangitis
Which of the following conditions is associated with sclerosing cholangitis?

A Autoimmune hepatitis
B Coeliac disease
C Irritable bowel syndrome
D Pernicious anaemia
E Ulcerative colitis (UC)
25. Investigation of status epilepticus

A 35-year-old homeless man presents to the emergency department in a
state of unconsciousness. He was fitting when the ambulance crew got to
him 20 minutes ago, and a friend at the scene estimated that he had started
fitting “around 15 minutes before”. His friend informed the ambulance
crew that he is a known epileptic and you find a pack of phenytoin on him.
He looks dishevelled and smells of alcohol. He has a blood pressure of
170/95 mmHg and temperature 37.9°C. On examination there is a quiet
systolic murmur, though it is difficult to fully characterise.
Which of the following investigations will be most useful at this stage?
A Computed tomography (CT) of the brain
B Echocardiogram
C Electroencephalogram (EEG)
D Magnetic resonance imaging (MRI) of the brain
E Phenytoin levels
26. Shortness of breath (1)

A 74-year-old male ex-comedian can no longer perform at smoky open-
microphone nights due to shortness of breath. He is coughing up frothy
white sputum, which recently has contained a small amount of blood.
On examination, his chest demonstrates diffuse crackles on inspiration
through which you can just discern a mid-diastolic murmur and a loud
first heart sound. His chest X-ray confirms pulmonary oedema.
What is the most likely underlying cause for his symptoms?
A Lower respiratory tract infection
B Mitral stenosis
C Non-small cell carcinoma of the lung
D Pulmonary embolism
E Small cell carcinoma of the lung
27. Aortic regurgitation

In clinic, a retired 62-year-old man presents with shortness of breath on
exertion. You find a collapsing pulse and subsequent echocardiography
8
confirms aortic regurgitation.
Which of the following is NOT associated with aortic regurgitation?

A Ankylosing spondylosis
B Aortic dissection
C Marfan syndrome
D Rheumatic fever
E Systemic lupus erythematosus (SLE)
28. Management of oliguria (1)

A previously fit and well 70-year-old woman has been admitted due to a
fractured neck of femur, and she has recently returned to the ward after
a cemented hemiarthroplasty. You are bleeped to the ward to see her, as
it is noted that she has had only 30 ml urine output in the last 3 hours.
She is asleep on the ward, with a patient-controlled analgesic device in
situ. Her airway is intact and her respiratory rate is 12/min with normal
saturations and good air entry bilaterally. Her pulse is 125 bpm with a
blood pressure of 95/68 mmHg and she has delayed capillary refill. She
has pale conjunctiva and a temperature of 37.3°C. She has a 12-hourly bag
of normal saline running. Her catheter is draining concentrated urine. An
abdominal examination is normal.
Which of the following interventions would you try first to increase the
urine output?
A Fluid challenge of 500 ml 5% dextrose over 10 minutes
B Fluid challenge of 500 ml normal saline over 10 minutes
C Flush the catheter
D Start antibiotics for presumed sepsis
E Stop the patient-controlled analgesic device
29. Steatorrhoea
A 23-year-old woman comes to see you about her stools, which over the last
couple of months have become extremely foul smelling, pale in colour and
difficult to flush. This has been associated with vague abdominal pains and
a bloating sensation. She has found this very embarrassing as she lives in a
shared house. She is normally fit and well.
A Chronic pancreatitis
B Coeliac disease
C Common bile duct obstruction
D Cystic fibrosis
E Giardia infection
9
30. Management of Parkinson’s disease (1)
An 83-year-old man who was diagnosed as having Parkinson’s disease 3

years ago has been treated with levodopa (L-DOPA). Whilst he initially
responded well to therapy, he has started to be increasingly still, and has
fallen more in the last 4 months despite no intercurrent illness or change
in L-DOPA therapy.
Which is the best management option?
A Add a dopamine agonist (e.g. ropinerole)
B Add a peripheral dopamine antagonist (e.g. domperidone)
C Decrease L-DOPA therapy
D Increase L-DOPA therapy
E Stop L-DOPA therapy
31. Autoantibodies
Which antibody can you expect to see in primary biliary cirrhosis (PBC)?
A ANA
B ANCA
C Anti-mitochondrial antibody
D Anti-phospholipid antibodies
E Anti-smooth muscle antibodies
32. Coronary circulation

The left anterior descending coronary artery usually supplies:
A The anterior wall of the left ventricle and the atrio-ventricular node
B The anterior wall of the left ventricle and the inter-ventricular septum
C The anterior wall of the left ventricle, atrio-ventricular node and the
inter-ventricular septum
D The inter-ventricular septum and the inferior part of the left ventricle
E The sino-atrial node, the atrio-ventricular node and the inferior part of
the left ventricle
33. Management of anaemia

A 42-year-old woman with menorrhagia is complaining of tiredness. The
GP does some blood tests, which reveal hypochromic microcytic anaemia,
a decreased ferritin level and a raised total iron binding capacity. Platelets
were slightly raised.
Which of the following is the best treatment for this anaemia?
A Erythropoietin
B Iron chelators
C Iron supplementation
D Regular transfusion
10
E Regular venesection
34. ACE inhibitors

In which of the following circumstances should angiotensin-converting
enzyme (ACE) inhibitors be avoided where possible?
A Glomerulonephritis
B Lupus nephritis
C Renal artery stenosis
D Systemic sclerosis with renal involvement
E All of the above
35. Microbiology
Which of the following correctly describes Staphylococcus aureus?
A Anaerobic rod
B Gram-negative coccus
C Gram-negative rod
D Gram-positive coccus
E Gram-positive rod
36. Skin lesions (1)

A 78-year-old retired groundskeeper presents with a 2 cm skin lump on his
temple. He is unsure how long it has been there. It appears to have a rolled,
shiny edge with telangiectasia and a central ulcerated area.
A Actinic keratosis
B Basal cell carcinoma
C Keratoacanthoma
D Malignant melanoma
E Squamous cell carcinoma
37. Diagnosis of abdominal pain (1)

A 54-year-old woman presents to the emergency department with a
2-month history of intermittent right upper quadrant pain. The pain is
sharp in nature and radiates round to the back. On examination there is no
jaundice, no hepatomegaly and she is apyrexial. Liver function tests and an
amylase are normal. She has no history of recent foreign travel.
A Biliary colic
B Cholangitis
C Hepatitis A
D Hepatitis C
E Pancreatitis
11
38. Ankylosing spondylitis
A 23-year-old man presents with a several-months history of lower back

pain and stiffness.
Which of the following symptoms would make you think of ankylosing
spondylitis (AS) as the diagnosis?
A Asymmetrical tenderness on palpation over the lumbosacral spine
B HLA-DR4 genotype
C Pain present on waking in the early morning
D Scoliosis present on examination
E Worse after heavy lifting
39. Mitral stenosis

A 75-year-old woman in the pre-assessment clinic tells you she has mitral
stenosis.
Which of the following is not a sign of mitral stenosis?
A Bifid P-wave
B Diastolic opening snap heart sound
C Double impulse apex beat
D Mid-diastolic murmur
E Peripheral cyanosis
40. Management of facial weakness

A 35-year-old man presents with a 2-day history of right-sided facial
weakness. He is otherwise fit and well. There is no past history of neurological
symptoms. There is no history of preceding infection. On examination, the
middle ear is normal, the salivary glands are not enlarged, and there are
no other cranial nerves affected. The forehead is not spared. Neurological
examination of the limbs is unremarkable. Routine investigations are all
normal.
Which of the following represents the most reasonable management plan?
A Aspirin, dipyridamole, a statin and an angiotensin-converting enzyme
(ACE) inhibitor
B Penicillin-based antibiotic therapy and antiviral therapy
C Steroids
D Steroids and penicillin-based antibiotic therapy
E Steroids, antiviral therapy and eye protection
41. Pathological fracture

A 51-year-old man is found to have a pathological fracture of his femur.
Investigations reveal immunoglobulin light chains in the urine.
12
What is his diagnosis?

A Benign monoclonal gammopathy
B Bone metastases
C Multiple myeloma
D Osteoporosis
E Vitamin D deficiency
42. Management of HIV

A 35-year-old man is diagnosed with human immunodeficiency virus
(HIV) infection.
Which of the following indicates that highly active antiretroviral therapy
(HAART) should be commenced?
A Fever and weight loss >10 kg
B Viral load >50 copies/ml
C Viral load >100 copies/ml
D CD4 count <200 cells/mm3
E CD4 count <500 cells/mm3
43. Tetralogy of Fallot

An anxious mum has read on the internet about tetralogy of Fallot as she is
convinced her little boy may have it.
Which of the following does not fit the diagnosis?
A Her child is small for his age
B Her child is cyanotic
C His pulse exhibits a radio-femoral delay
D Her child exhibits a loud systolic murmur
E Her child can relive symptoms just by squatting
44. Investigation of dysphagia

A 45-year-old man presents with intermittent difficulty in swallowing
for the last 4 months. This is associated with severe retrosternal pain and
regurgitation. He has no risk factors or sinister signs for malignancy.
What is the most important investigation in this case?
A Barium swallow
B Chest X-ray
C CT of the chest
D Endoscopy
E Iron studies
13
45. Thalassaemia trait
A 55-year-old Asian man with known thalassaemia trait registers with a

new GP and is found to have a mild microcytic anaemia on routine testing.
He does not complain of any symptoms.
What is the most appropriate treatment?
A Blood transfusion
B Folate supplementation
C Iron chelators
D Iron supplementation
E No treatment required
46. Warfarin therapy

A 72-year-old man is on warfarin for atrial fibrillation. Following a recent
chest infection his international normalised ratio (INR) rockets up to 5.2.
What was the most likely cause for this?
A Codeine phosphate
B Erythromycin
C Inappropriate high doses of warfarin
D International normalised ratio (INR) increased in concomitant infection
E Steroid inhalers
47. The painful joint

A 40-year-old man, previously fit and well, limps in to the emergency
department with an acutely red, hot, swollen, exquisitely tender knee,
which he holds rigid. He is tachycardic and has a temperature of 38.3°C.
Which of the following represents the best approach to diagnosis and
management?
A Aspirate a small amount of joint fluid and send it for microscopy under
polarised light
B Aspirate a small amount of joint fluid, send the fluid for urgent Gram
stain and culture, take blood cultures, and start antibiotics only when you
know the sensitivities of any bacteria present
C Aspirate the joint fully, send the fluid for urgent Gram stain and culture,
take blood cultures, and start antibiotics only if bacteria are detected on
Gram stain of either fluid
D Aspirate the joint fully, send the fluid for urgent Gram stain and culture,
take blood cultures, and start antibiotics only when you know sensitivities
of any bacteria present
E Aspirate the joint fully, send the fluid for urgent Gram stain and
culture, take blood cultures, and start empirical intravenous antibiotics
14 immediately
48. The unresponsive patient (1)

A 29-year-old man is brought to the emergency department having been
found unresponsive on a park bench. On examination, his airway is patent
and he has a spontaneous respiratory rate of 7, with a saturation rate of
92% on air. There is no abnormality on examination or auscultation of the
chest. He has a pulse of 70 bpm and a blood pressure of 110/80 mmHg. The
ECG is normal. He has a Glasgow Coma Score (GCS) of 3 and has pinpoint
pupils. He has a temperature of 36.8°C and a blood sugar reading of 6.
Basic initial management steps include high-flow oxygen administration
and intravenous access.
Which of the following might you also implement?
A 500 ml stat intravenous fluid challenge
B 50 ml of 50% glucose intravenously stat
C Bair hugger
D Flumazenil
E Naloxone
49. Vomiting
A first-time mother comes to visit you with her 10-month-old son. At
least once every day her son vomits up his entire feed. The vomiting is not
projectile but rather the feed returns to the mouth and spills over his top.
She stopped breast-feeding him when he was 6 months old. He is otherwise
well in himself, with a normal weight for his age.
A Gastro-oesophageal reflux disease
B Lactose intolerance
C Physiological posseting
D Pyloric stenosis
E Viral gastroenteritis
50. Weight loss

A 13-year-old girl, who is quiet and withdrawn, comes to see you with
her mother. She has a 4-month history of weight loss and secondary
amenorrhoea. She has no bowel symptoms. Her body mass index is 16.
Apart from being very thin, the examination is otherwise normal. All blood
results, including hormone assays, are normal.
A Anorexia nervosa
B Coeliac disease
C Crohn’s disease
D Epstein–Barr virus infection
15
E Irritable bowel syndrome
Practice Paper 1: Answers
1. Acute coronary syndrome (1)
B. Give 75 mg aspirin stat
A stat dose of 300 mg aspirin is the correct figure. Low-dose (75 mg)
aspirin is used for long-term prevention. ACS is the title given to a
collection of cardiac diseases that all share the same atherosclerotic
aetiology. ST-elevated MI, non-ST-elevated MI and unstable angina are
all caused by stenosed coronary arteries starving the myocardium of
oxygen (angina), leading to hypoxic cell death (myocardial infarction).
Unstable angina occurs on the cusp of these phenomena, when a
rest is no longer adequate to replenish the myocardium with oxygen.
Acute coronary stenoses are usually caused by intimal plaque rupture
leading to an intraluminal thrombus. Aspirin, clopidogrel and heparin aim
to prevent platelets binding and therefore to arrest thrombus growth and
dissolve the thrombus. Aspirin can cause stomach ulcers and so, in order to
balance risks and benefits, low-dose aspirin is given long term; a higher dose
(300 mg) is given acutely. Statins prophylactically lower serum cholesterol,
and so it is thought to reduce plaque formation in the first place. ACE
inhibitors and beta-blockers reduce afterload and heart rate, so the heart
does not have to work as hard – this lowers its oxygen demand, hopefully
enough to prevent hypoxic damage.
2. Obstructive renal impairment

E. Systemic sclerosis
Benign prostatic hypertrophy can cause urinary retention and increased
pressure in the urinary outflow tract, and as this disease affects older men,
who can be quite reluctant to seek help with non-urgent medical problems,
this can get to the stage at which kidney function is impaired. Recurrent
kidney stones passing into the ureter can cause scarring, especially at narrow
sites such as the vesicoureteric junction. Retroperitoneal fibrosis typically
involves a fibrosing inflammatory reaction starting in the wall of the aorta
and spreading retroperitoneally. The ureters can become embroiled in the
fibrous tissue. Obstruction is believed to be due to a loss of peristalsis rather
than occlusion. Schistosomiasis is common in the Middle East and parts
16
of Africa, featuring granulomas forming around the eggs of schistosomes
in the urinary tract, and these can obstruct the urinary tract. Systemic

sclerosis leads to a fibrinoid thickening of the afferent arterioles, leading to
reduced renal perfusion and thus renal impairment, but it does not cause an
obstructive uropathy.
3. Management of skin lesions (1)

A. Cryotherapy
This man has a past history of likely excessive sun exposure and thus is at risk
for sun-related skin disease. This lesion appears to be an actinic keratosis – it
is not pigmented (effectively ruling out melanoma), and it is flat rather than
raised, making basal cell and squamous cell carcinomata unlikely (although
there can be superficial basal cell carcinomas, which are well demarcated
and deep red, with less scale). A small mildly erythematous patch with
keratotic hypertrophy (scales and horns) is most likely an actinic keratosis
(or solar keratosis). Treatment of isolated small lesions is by cryotherapy.
It has no concerning features to suggest that excision or histopathological
examination is required. Large areas of skin with multiple actinic keratoses
can be treated with 5-fluorouracil cream to avoid excessive scarring from
cryotherapy, and can be more effective at slowing re-growth.
4. Chest X-ray
A. Trachea deviated to the right, dull to percussion of RUZ, reduced
breath sounds on auscultation
A lung collapse would tend to pull the trachea towards the affected side.
There would be reduced breath sounds (with or without crackles and
bronchial breathing) and dullness to percussion on the affected side.
5. Headaches
D. Polycythaemia rubra vera
Polycythaemia rubra vera is a myeloproliferative disorder characterised by a
raised haemoglobin level, red cell count and packed cell volume (haematocrit).
The condition is caused by the mutation of a single pluripotent stem cell, which
results in the excessive production of erythrocytes and, to a lesser degree,
platelets and neutrophils. As a result, the blood becomes extremely viscous
causing an increased risk of arterial and venous thrombosis and paradoxical
bleeding. Patients often complain of headaches, visual disturbance, lethargy
and pruritis that is classically worse after bathing in warm water. Treatment
of the polycythaemia rubra vera involves venesection (blood-letting) and
chemotherapy with hydroxyurea. If treated appropriately patients tend to
17
survive for many years and often die from non-related causes. Approximately
30% of patients will develop myelofibrosis and 5% will develop acute myeloid
leukaemia as part of the disease’s natural history.

Secondary polycythaemia is usually caused by the increased secretion of
erythropoietin as part of the physiological response to hypoxia in conditions
such as chronic obstructive airways disease and cyanotic heart disease. Less
frequently erythropoetin is secreted ectopically from tumour cells (e.g. renal
cell carcinomas). Occasionally the condition is iatrogenic, caused by the
overuse of artificial erythropoietin used in the treatment of conditions such
as anaemia of chronic renal failure. Investigating polycythaemia involves
referral to a haematologist, who will accurately assess the red cell mass
and exclude secondary causes. Bone marrow analysis may be required to
diagnose genetic abnormalities. The treatment of secondary polycythaemia
involves managing the underlying disease and symptomatic venesection.
Polycythaemia, from Greek poly = many + kytos = cell
Rubra vera, from Latin rubra = red + vera = true
6. Chronic obstructive pulmonary disease

B. Inhaled corticosteroids
Smoking cessation is important in patients with chronic obstructive
pulmonary disease and it is the only intervention proven to decelerate the
decline in FEV1. Pneumococcal and annual influenza vaccination is provided
to reduce the risk of exacerbation of chronic obstructive pulmonary disease
(COPD) by viral infection. Short-acting bronchodilators (e.g. b2 agonists or
anticholinergics) help in reducing breathlessness and exercise limitation. A
combined therapy of these two bronchodilators is used if the patient is still
symptomatic with just one type of inhaled bronchodilator. A long-acting
bronchodilator is added if symptoms persist with the combined therapy.
Inhaled corticosteroids are added if FEV1<50% and the patient has two or
more exacerbations in a 12-month period.
7. Management of asthma (1)

D. Leukotriene receptor antagonists
The altered level of consciousness, exhaustion, silent chest, PaO2 <8.0 kPa,
and “normal PaCO2” 4.6–6.0 kPa all suggest that this patient has life-
threatening asthma. High-flow oxygen is needed to maintain a saturation
level of 94–98%. In acute life-threatening asthma, the nebulised route
(oxygen driven) is recommended. Steroids reduce mortality, relapses,
subsequent hospital admission and requirement for beta-2 agonist therapy.
Magnesium sulphate has bronchodilation effects and is used in acute severe
18 asthma if there is not a good initial response to inhaled bronchodilator
therapy, and also in life-threatening asthma. There is insufficient evidence

at present to show that leukotriene receptor antagonists are effective in the
management of acute asthma.
8. Collapse (1)
B. Hypertrophic obstructive cardiomyopathy (HOCM)
HOCM is a congenital disease of the myocardium. The left ventricular
myocardium becomes so thick that the outflow tract becomes restricted.
This restriction is mechanically exacerbated by the muscular systolic
contraction generated by vigorous exercise, hence, hard exercise leads to a
fall off in output, which leads to syncope. Sufferers are vulnerable to sudden
death, of which there may be a family history as the disease is inherited
(autosomal dominant).
9. Eczema versus psoriasis

C. Localised to flexures rather than extensors
Whilst nail pitting and ridging may occasionally be seen with eczema, nail
changes are much more commonly associated with psoriasis, usually with
nail pitting and onycholysis (detachment of parts of the nail from the nail
bed), and occasionally with subungual hyperkeratosis (extensive keratotic
growth beneath the nail). Distal interphalangeal joint disease (in this case
with pain and swelling) is one of five characteristic patterns of ‘psoriatic
arthropathy’, which overall around 5–10% of those with psoriasis will
develop at some stage – in some cases, before the outbreak of psoriasis. The
five patterns are distal interphalangeal arthritis, symmetrical polyarthritis,
asymmetrical oligoarthritis, spondyloarthropathy and arthritis mutilans,
which is a severe destructive arthropathy mainly affecting the hands.
Eczema is more commonly localised to flexures, whereas psoriatic
plaques are more typically localised to extensor surfaces. That said, there
is a variety of psoriasis that more often develops later in life, in which the
plaques appear in well-opposed flexural surfaces such as the groin and
submammary area. Psoriasis more often presents with well-demarcated
lesions or “plaques”, whereas eczematous lesions more often are described
as “patches”. Psoriasis typically responds well to sunlight and thus would
be worse in the winter months. This is the basis of ultraviolet (UV) therapy
for psoriasis, and patients may be advised to expose affected skin (within
reason) to sunshine where possible – although this is often difficult due to
cosmetic concerns.
19
10. Diagnosis of multiple sclerosis (1)
D. Periventricular white matter lesions not necessarily matching the

clinical picture
Longitudinally extensive transverse myelitis is unusual in multiple sclerosis
(MS), and is more typical of neuromyelitis optica (NMO or Devic disease),
a rare autoimmune central nervous system demyelinating disease affecting
the spinal cord and optic nerves. Once thought to be a subtype of MS,
however, it is now known to be a distinct disease strongly associated with
anti-aquaporin 4 antibodies. Whilst grey matter is affected in MS, and
there is some evidence that overall grey matter volume decreases in MS and
correlates with disability, focal grey matter inflammatory lesions would not
be expected, and the focal lesions are in fact found in the white matter. The
cerebellum and brainstem are affected in multiple sclerosis, however, not
exclusively. White matter lesions are classically described as “periventricular”,
and the lesions found do not always correlate with a clinical focus of disease.
This is because the central nervous system (CNS) inflammation does not
always cause demyelination or axonal damage of clinical significance, and
the CNS can recover from these foci of inflammation.
Eugene Devic, French neurologist (1858–1930)
11. The multidisciplinary team

A. District nurse
District nurses provide care within the community. Their workload includes
looking after house-bound and recently discharged patients, helping them
manage wound dressings and monitor medications.
Social workers look after the individuals and their contacts from a social
perspective (e.g. families, friends). They also liaise with other organisations
including schools, the National Health Service (NHS), housing agencies
and charitable organisations to plan packages of care and support for the
individual. The health visitor (a qualified nurse) takes over care of a newborn
from community midwives after the first 10 days of birth. Health visitors
also run health promotion and smoking cessation clinics. An orthotist is
someone who measures, designs and fits orthoses (an external device that
can be applied to correct a deformity, rather like a splint).
Orthotics, from Greek ortho = straighten
12. Diagnosis of chest pain (1)

E. I’m not sure, we need to do more tests
This man has left bundle branch block (LBBB). The ST elevation does not
20
therefore confirm MI as the ST elevation could be due to the abnormal left
ventricular depolarisation. If the clinical features are in keeping, he could be

treated for a presumed myocardial infarction until 12-hour troponin blood
test results are available to confirm or deny the diagnosis and/or other ECG
changes appear, such as pronounced Q-waves growing over time. Bundle
branch block can be remembered by: WiLLiaM and MaRRoW. LBBB (the
“L”s in WiLLiaM) is reported by a broad S-wave (or deep Q- and S-waves)
in the right-hand leads (forming a “W” in the QRS of V1–3, mainly V1)
and a pair of R-waves in the left-hand leads (forming an “M” in the QRS of
V4–6, mainly V6). Either way, the QRS complexes will be broad, even if the
“W”s and “M”s are not obvious. Right bundle branch block (RBBB) reports
the reverse: an “M” in the QRS of leads V1–3 and a “W” in the QRS of
V4–6.
Other causes of a LBBB include aortic stenosis, dilated cardiomyopathy,
chronic hypertension and extensive coronary artery disease without MI.
The finding of LBBB is always pathological. New LBBB with typical features
is consistent with the diagnosis of an acute coronary syndrome.
13. Risk factors for ischaemic heart disease

E. 12 U/week of alcohol
Moderate alcohol consumption can reduce coronary artery disease but heavy
drinking increases it. All the other options increase the risk of ischaemic
heart disease and are modifiable.
14. Diagnosis of cough (1)

C. Legionella pneumophila
Legionella pneumophila tends to colonise in water tanks kept at below 60°C
(e.g. hotel air-conditioning and hot water systems). Patients who acquire
Legionella pneumophila infection will present with non-specific symptoms
such as fever, myalgia, headache, confusion and diarrhoea. Blood tests
reveal hyponatraemia, abnormal liver function tests (elevated liver enzymes,
hypoalbuminaemia) and an elevated creatine kinase. The diagnosis is
confirmed by Legionella serology or urine Legionella antigen.
15. Diagnosis of vertigo

B. Delayed onset (a few seconds) torsional nystagmus on descent facing
one side only
Benign paroxysmal positional vertigo (BPPV) is caused by debris blocking
the normal flow of endolymph in the labyrinth, leading to misreporting
of positional change by the vestibules, and a discrepancy between actual
21
position and the position of the head according to the vestibules. Thus,
nystagmus occurs as two different inputs compete for different oculomotor
outputs, and vertigo (the perception that the world is moving) ensues.
This happens only when the head moves and there is no vertigo with a
still head. It usually affects one side only, and thus Hallpike’s manoeuvre
(below) only reveals nystagmus when the patient’s head is tilted back whilst
they face one side and not the other. Torsional nystagmus is normally seen
after a few seconds of the head being tilted back – it is important to keep
the patient lying back for some time. The nystagmus should wear off after
around 20 seconds, and on repeat testing it lasts a shorter amount of time
(“fatiguing”). This is the basis of vestibular exercises, which are designed
so that compensatory mechanisms may be induced more swiftly and the
vertigo attacks will thus become less frequent and less disabling.
The Hallpike test is conducted as follows:
1. The patient sits upright with their legs extended.
2. The patient’s head is then rotated 45 degrees.
3. The patient is then made to lie down quickly and the head is held in
extension.
4. The patient’s eyes are then observed. A positive test will result in nystagmus
towards the affected side after a 5–10 second latent period.
The Epley manoeuvre effectively treats most cases of BPPV. In this
manoeuvre:
1. The patient sits upright with their legs extended.
2. The patient’s head is rotated towards the affected side.
3. With the head still turned, the patient is laid flat past the horizontal (as in
the Hallpike test). This position is held for 30 seconds.
4. The patient’s head is then turned to the opposite side in the reclined
position (and held for 30 seconds).
5. The patient is now rolled onto their side (the side opposite to the affected
ear) with the head still turned for 30 seconds.
6. The patient is then made to sit upright, still with the head turned to the
opposite side of the lesion (for 30 seconds).
7. The patient’s head is turned back to the midline with the neck flexed 45
degrees (for 30 seconds).
Charles Skinner Hallpike, English otologist (1900–1979)
16. Epistaxis
E. Wegener granulomatosis
Wegener granulomatosis is characterised by systemic vasculitis that involves
small and medium vessels. The classic triad consists of upper and lower
respiratory tract involvement and pauci-immune glomerulonephritis. The
22
upper respiratory tract involvement includes otorrhoea, sinusitis, nasal
discharge and crusting, epistaxis, oral and nasal ulcers, mucosal bleeding

and inflammation, nasal septal perforation and a saddle nose deformity. The
lower respiratory tract involvement includes cough, haemoptysis, chest pain
and shortness of breath. Microscopic haematuria is a common finding in
Wegener granulomatosis. A positive ANCA test in the setting of this classic
triad is sufficient to diagnose Wegener granulomatosis without a histological
confirmation. Goodpasture syndrome is caused by an anti-glomerular
basement membrane antibody that results in pulmonary haemorrhage and
glomerulonephritis without involvement of the upper respiratory tract.
Friedrich Wegener, German pathologist (1907–1990)
17. Diarrhoea (1)

B. Clostridium difficile infection
C. difficile is a major cause of antibiotic-association diarrhoea and hospital
morbidity within the country. C. difficile is a Gram-positive commensal
bacterium of the gastrointestinal tract that can proliferate when the intestinal
flora is disturbed by the use of broad-spectrum antibiotics. Third-generation
cephalosporins were particularly implicated with this and their use is not
advised in the over 65s. C. difficile produces two enterotoxins (A and B) that
cause severe inflammation of the intestinal mucosa and the formation of
thick fibrous bands (pseudomembranes) in the intestine, which can harbour
large numbers of bacteria. The patient often has significant diarrhoea
(with or without blood), which can lead to rapid dehydration, electrolyte
imbalance and death. C. difficile is treated by managing the patient’s fluid
and electrolyte balance and prescribing a course of metronidazole or
vancomycin. Much effort is being placed in the prevention of Clostridium
infection by promoting the correct use of broad-spectrum antibiotics and
educating staff and visitors regarding the importance of hand washing. It
should be noted that the spores of C. difficile are not destroyed by alcohol
hand gel, meaning that soap and water must be used every time!
Clostridium, from Latin kloster = spindle (shape)
Difficile, from Latin difficile = difficult
18. Diagnosis of malaria

E. Three thick and thin blood films on consecutive days
Falciparum antigen dipstick testing is a useful, cheap and labour-unintensive
way to diagnose or exclude falciparum malaria, however, a well-examined
blood film is far more sensitive. Thick and thin blood films are done because
thick films make pickup of low-level parasitaemias more likely and thin
23
blood films allow species identification and quantification (more than 2%
of red blood cells being parasitised is a prognostic marker of severe disease).
Blood films should be taken on 3 consecutive days, as an initial film may be

negative due to the lifecycle of the parasite. Blood cultures should be taken
as there may be coexisting bacteraemia (“algid malaria”), however they do
not grow Plasmodium species. Liver biopsy is not used to investigate malaria.
19. Electrocardiogram (1)

A. First-degree heart block
Analyse an ECG methodically. Start with rate: bradycardia if less than 60/
min, tachycardic if greater than 100/min. Next, check the rhythm is regular;
this can be trickier than it seems, especially if the patient is tachycardic.
The axis is determined by looking at the amplitude of the QRS complex
relative to lead II, i.e. lead II is 0°, lead I is –45° and lead III is +135°. If the
QRS amplitude is greatest in lead II and leads I and III have identical, lesser
magnitudes, then the QRS is not deviated. If it is most positive in lead I, then
it is deviated to the left. If it is most positive in lead III, then it is deviated to
the right. Remember that the QRS complex is the charge “washing” through
the myocardium. The axis of the QRS helps us to visualise the comparative
muscularity of the right and left ventricles, which may in turn highlight a
disease process against which a given ventricle is fighting, e.g. aortic stenosis
leading to left ventricular hypertrophy resulting in left axis deviation. An
axis outside of ±30 degrees can be said to be deviated. The P-wave position
and shape should be noted. The PR interval should be less than 0.20 seconds.
In this case, there is a fixed delay (through the atrio-ventricular node) which
is called first-degree heart block. QRS amplitude, shape and duration are all
significant. A width >3 small squares (at 25 mm/s ECG speed) is equivalent
to 0.12 seconds, and this is the boundary between QRS complexes being
narrow or broad. Ventricular tachycardias are broad (and faster than 90/
min). A broad complex may well contain a distortion in shape in one of the
leads indicating bundle branch block. This ECG has a narrow QRS complex.
Finally, the T-wave size and the QT duration should be observed. It is always
good practice to compare a current ECG to a previous ECG but this should
not prevent you reviewing and summarising the ECG. If there is any doubt,
and no old ECGs are available, a repeat test can be requested.
20. Investigation of deranged liver function tests

A. Alpha-1-antitrypsin serum levels
Alpha-1 antitrypsin (A1AT) deficiency is an autosomal recessive disorder.
About 1% of COPD patients will have this genetic abnormality. A1AT is a
serine protease inhibitor normally synthesised in the liver whose role is to
cleave and inhibit the proteolytic enzyme neutrophil elastase. Absence of
24
A1AT leads to pulmonary emphysema and liver disease in some patients.
The gene is located on chromosome 14 and there are variants that correlate

to disease severity and presentation. The most severe forms can present with
cirrhosis in childhood. Treatment is supportive.
21. Epigastric pain (1)

A. Acute pericarditis
The ECG shows widespread saddle-shaped ST elevation, a typical change
associated with acute pericarditis. Viral pericarditis can be caused by a
preceding viral respiratory tract infection; bilateral pulmonary effusions
may also be present. Pleurisy – inflammation of the pleura – does not directly
cause ECG changes and does not correlate as well with the sign of postural
pain changes. Myocardial infarction and angina are unlikely to cause pain
of this nature, but a 12-hour troponin test should be requested. A painful
pulmonary embolism would usually affect the oxygen saturations and not
necessarily provide ECG evidence. If in doubt, blood gas testing should be
undertaken.
22. Gout prophylaxis

C. Start allopurinol at least 2 weeks after the acute attack has settled
with NSAID cover and increase until his urate level is below 300 μmol/L
Long-term diclofenac carries the risk of side effects such as peptic ulceration
and renal impairment, and will achieve nothing between attacks as there
is no inflammation. Similarly, depot steroid injections may be used in
acute attacks but long-term steroids carry the risk of immunosuppression
as well as many other side effects. The underlying pathology in gout is
hyperuricaemia, therefore prophylactic treatment should aim to reduce
serum urate. Allopurinol inhibits xanthine oxidase, which produces urate,
and thus lowers serum urate. It can precipitate acute attacks and therefore
should not be used within 2–4 weeks of an acute attack, and should be started
with either NSAIDs or colchicine used at least 2 weeks before and 4 weeks
after starting. Long-term colchicine is not recommended for prophylaxis.
Sulfinpyrazone is a second-line prophylactic agent.
23. Hepatomegaly
A. End-stage cirrhosis
Hepatomegaly describes the enlargement of the liver. It is detected clinically
by palpating the right upper quadrant during inspiration. As the patient
inspires the liver is displaced inferiorly by the lungs onto the examiner’s hand.
In normal individuals the liver should not be palpated with the exception
25
of children and particularly thin patients. The presence of hepatomegaly is
usually described in terms of size, e.g. number of finger-breadths below the
costal margin. The texture of the liver edge should also be documented and
it should be noted whether it is smooth or craggy. Conditions that cause
hepatomegaly with a smooth margin include viral hepatitis, biliary tract
obstruction, hepatic vein thrombosis (Budd–Chiari syndrome), right heart
failure and myeloproliferative disease. Hepatomegaly with a craggy border
is usually associated with hepatic metastatic disease and polycystic disease.
End-stage cirrhosis does not result in hepatomegaly. Early liver damage often
causes hepatomegaly and fatty infiltration, but as the damage progresses and
fibrosis ensues, replacing the normal tissue architecture, the liver becomes
small and scarred.
24. Sclerosing cholangitis

E. Ulcerative colitis (UC)
Sclerosing cholangitis is a condition causing inflammation, fibrosis and
subsequent stricture formation of the bile ducts, leading to cholestasis and
eventual cirrhosis. These changes occur in the intra- and extrahepatic bile
ducts. There is a strong association with inflammatory bowel disease, most
commonly ulcerative colitis, with about 80% of patients with sclerosing
cholangitis having coexistent disease (note that although only ~5% of
patients with UC have concomitant sclerosing cholangitis). These patients
present with the effects of jaundice. Liver biopsy is diagnostic. Treatment is
primarily symptomatic. Ursodeoxycholic acid may delay disease progression
and liver transplant is curative in some cases. Purely extrahepatic disease
may be surgically treated.
25. Investigation of status epilepticus

E. Phenytoin levels
There are many reasons why this man may be in status epilepticus, but the
most common cause, and a quick and simple one to rule out, would be low
antiepileptic drug levels. This is estimated to be the cause of around 30% of
status episodes. Alcoholism is prevalent amongst the homeless population,
and many antiepileptics are metabolised by the cytochrome p450 system in
the liver (phenytoin included). Chronic alcohol abuse can induce increased
cytochrome p450 activity, which could then lower the phenytoin levels.
His compliance with phenytoin therapy could be poor given his social
situation. Regarding the other investigations, brain imaging will be poor or
impossible as he is still fitting, and EEG is only indicated if he is still fitting
after various management steps have been undertaken and he is taken to
the intensive treatment unit (ITU) for general anaesthesia. Regarding the
26
echocardiogram, the homeless population is indeed at risk of endocarditis,
which could lead to subsequent septic embolisation to the brain, causing the

seizures. A murmur is also heard, however this would be a less likely cause
than low phenytoin levels, and less easy to treat acutely if found. Magnetic
resonance imaging (MRI) of the head should be carried out beforehand if an
intracranial cause such as septic emboli is being considered. Furthermore,
regarding the possibly new murmur and fever, the fever could be due to the
seizure activity, and the murmur could be benign or old (it may be worth
contacting the GP or searching for the patient’s old hospital notes to see if it
has been investigated).
26. Shortness of breath (1)

B. Mitral stenosis
A history of recurrent rheumatic fever would reinforce this diagnosis. This
patient’s mitral valve is restricting the onward flow of freshly oxygenated
blood from the lungs. This back-pressure is the cause of his pulmonary
oedema (inspiratory crackles, frothy pinky–white sputum). The loud first
heart sound is due to the mitral valve leaflets shutting abruptly at the start
of systole, as if a door ajar were closed with the same force as a door wide
open. The mid-diastolic murmur is the turbulent flow of blood through
the restricted opening. It is low-frequency and so is best heard with the
bell of the stethoscope. A malar flush may be visible upon the face of
the patient.
Rheumatic fever is predominantly a disease of the developing world, and
is usually seen in children between 5 and 15 years of age. The condition
develops 2–4 weeks after a group A beta-haemolytic streptococcal
pharyngitis. In susceptible individuals, the antibodies formed against the
bacterial carbohydrate cell wall cross-react with antigens in the heart, joints
and skin in a process known as molecular mimicry. The immune response in
the heart causes myocarditis, pericarditis and endocarditis, resulting in valve
destruction, conduction defects, arrhythmia and congestive cardiac failure.
The diagnosis of rheumatic fever is made using the modified Duckett Jones
criteria, requiring either two major criteria OR one major and two minor
criteria PLUS evidence of streptococcal infection (e.g. anti-streptolysin-O
titres):
Modified Duckett Jones criteria
Major
Pancarditis
Polyarthritis
Sydenham chorea (St Vitus’ dance)
Erythema marginatum
27
Subcutaneous nodules
Minor
Fever
Arthralgia
High erythrocyte sedimentation rate or white cell count
Heart block
Chorea, from Latin chorea = dance
Saint Vitus’ dance (chorea sancti viti in Latin) was a mediaeval festival that
celebrated Vitus, the patron saint of dancers, actors and comedians
T Duckett Jones, American physician (1899–1954)
27. Aortic regurgitation

E. Systemic lupus erythematosus (SLE)
SLE can cause myocarditis, pericarditis and endocarditis. Whilst the latter
manifestation can cause valvular vegetations, they are rarely symptomatic
and are more likely to be diagnosed post mortem. Causes of aortic
regurgitation, which presents primarily as dyspnoea, include idiopathic
aortic root dilatation, syphilitic aortitis, aortic dissection and rheumatic
fever. It is also associated with ankylosing spondylosis and Marfan syndrome.
In addition to a collapsing pulse, aortic regurgitation also presents with an
early diastolic murmur, a mid-diastolic rumble (Austin Flint murmur), de
Musset’s sign (synchronous head nodding), Quincke’s sign (pulsing nail
bed), Traube’s sign (“pistol shot” sound at the femoral artery as its walls
slacken and then crack taught like a sail in the wind) and a laterally displaced
apex beat.
Austin Flint, American physician (1812–1886)
Alfred de Musset, French novelist who died from aortic regurgitation.
His brother noticed his head used to bob with his pulse
Heinrich Irenaeus Quincke, German physician (1842–1922)
Ludwig Traube, German physician (1818–1876)
28. Management of oliguria (1)

B. Fluid challenge of 500 ml normal saline over 10 minutes
It is likely that there has been a fair bit of blood loss intraoperatively. The
operation notes could be checked to confirm this. It is major orthopaedic
surgery and she has conjunctival pallor, which make it seem fairly likely. She
seems clinically dry with tachycardia, reduced blood pressure and delayed
capillary refill, which follows on from the intraoperative blood loss with
28
slow intravenous fluid replacement (12 hourly). She could also theoretically
be septic, but low-grade pyrexia is common postoperatively and there is no

presumed source. A urine dip test could be taken to rule out urine infection.
Hypovolaemia is more parsimonious. She does not have heart failure and
should be able to tolerate a fluid challenge; this is a quick way to find out
whether hypovolaemia was to blame. Normal saline should be used rather
than 5% dextrose, as the saline will remain largely intravascular, whereas
the 5% dextrose, after rapid metabolism of the dextrose, is essentially water,
and this will enter the tissues and not increase the intravascular volume as
much. Intravenous fluids could then subsequently be sped up. Flushing the
catheter can rule out obstruction of the catheter, but the bladder was not
palpable on examination and there was no previous bleeding to suggest
potential obstruction; this is quick and does not harm the patient so could
also be tried. Morphine does not commonly reduce urine output or lead to
renal failure. It can cause urinary retention, however a catheter is in situ so
this is not the cause here.
29. Steatorrhoea
B. Coeliac disease
The description of this woman’s stools is classical for steatorrhoea, which is a
malabsorption of fat from the diet. There are many causes for this including
all of the above. However, coeliac disease is the most likely diagnosis in a
woman of this age group with no other symptoms of respiratory distress
or foreign travel. If the diagnosis is in doubt then repeated stool specimens
should be sent for Giardia cysts and ova identification.
30. Management of Parkinson’s disease (1)

A. Add a dopamine agonist (e.g. ropinerole)
The general theory of Parkinson’s disease management is that early on,
when there are still many SNpc neurons surviving, L-DOPA is more useful
as this precursor then increases the amount of dopamine being released
in a physiological manner to allow movement. However, as the disease
progresses and the SNpc neurons reduce in number, L-DOPA increases will
not be able to increase the functional amount of dopamine being released
in the basal ganglia and so dopamine agonists should increasingly be used.
This is less physiological but improves bradykinesia. At the latter stage,
increasing L-DOPA is unlikely to provide a benefit; decreasing L-DOPA may
be advisable but not without a dopamine agonist, and stopping it altogether
is likely to worsen function. The addition of a dopamine agonist may relieve
bradykinesia and postural instability at this stage. A peripheral dopamine
antagonist: 1) will not act centrally and 2) would exacerbate symptoms, so
would be no help. Domperidone can in fact be used to relieve medication-
29
associated nausea in Parkinson disease.
31. Autoantibodies
C. Anti-mitochondrial antibody
PBC is a rare condition predominantly affecting women in their 50s. The
aetiology is thought to be autoimmune. There is chronic granulomatous
inflammation of the interlobular bile ducts causing cholestasis. Presentation
is through the effects of cholestasis – jaundice, pruritis, hepatomegaly
and pain. It may also be picked up early by deranged liver function tests
in the asymptomatic patient. Diagnosis is made by liver biopsy, and anti-
mitochondrial antibodies may be present. Management is threefold: 1)
symptomatic to reduce itchiness and prevent osteoporosis, 2) specific
medications to improve absorption and finally 3) disease-modifying drugs
such as ursodeoxycholic acid (which reduces cholestasis). Recent evidence
however suggests that ursodeoxycholic acid does not improve mortality.
Liver transplant may be an option in some candidates with end-stage disease.
32. Coronary circulation

B. The anterior wall of the left ventricle and the inter-ventricular septum
The left anterior descending artery normally supplies the anterior wall of
the left ventricle and the inter-ventricular septum. It arises from the left
coronary artery, as does the circumflex artery, which supplies the posterior
and lateral sides of the left ventricle. The right coronary artery usually
supplies the sino-atrial node, atrio-ventricular node, right ventricle and
inferior part of the left ventricle.
33. Management of anaemia

C. Iron supplementation
These blood tests reveal iron-deficiency anaemia, which is most commonly
treated with oral iron supplementation.
Iron deficiency anaemia (IDA) is defined as a haemoglobin concentration
below 13.5 g/dL in males or 11.5 g/dL in females, in association with a
low mean cell volume (MCV) and evidence of depleted iron stores (i.e.
a low ferritin and a raised total iron binding capacity). In the developed
world IDA is usually secondary to chronic blood loss from gastrointestinal,
uterine and urinary tract sources. (Worldwide, hookworm infection and
schistosomiasis are common causes.) In cases where the source of bleeding
is obvious, further investigation is usually not necessary and treatment can
begin; however in many instances bleeding goes unnoticed and is secondary
to a more sinister cause such as gastrointestinal malignancy. As such, patients
with IDA without an obvious cause must be referred for investigation of the
30
upper and lower gastrointestinal tract in the first instance.
To treat IDA the underlying cause must be corrected and iron stores replen-

ished. The most appropriate method of replacing iron is with oral supple-
mentation (e.g. ferrous sulphate 200 mg tds). Haemoglobin should rise by
1 g/dL every 7 days. Treatment is given until haemoglobin concentrations
return to normal and for a further 3–6 months in order to replenish the de-
pleted iron stores. If the haemoglobin fails to respond as expected you must
consider non-compliance/concordance with treatment, malabsorption and
misdiagnosis. Intramuscular and intravenous preparations of iron do exist
but are usually reserved for cases of refractory anaemia secondary to malab-
sorption and chronic disease. Blood transfusion should only be considered in
severe and symptomatic anaemia (e.g. Hb <8 g/dL). Expect the haemoglobin
concentration to increase by 1 g/dL per unit of red blood cells given.
34. ACE inhibitors

C. Renal artery stenosis
Glomerulonephritis and lupus nephritis are both autoimmune in origin
and aside from supportive measures and renoprotection with drugs
including ACE inhibitors, immunosuppression is commonly used and
works with varying effect. Systemic sclerosis can affect the afferent arterioles
with fibrinoid thickening and vessel narrowing, which can come on rapidly
(“scleroderma renal crisis”). Immunosuppression is often unhelpful,
whereas ACE inhibitors are of immense benefit and can halt progression of
loss of renal function and sometimes even partially reverse it. In severe renal
artery stenosis, ACE inhibitors can further reduce or abolish glomerular
filtration. This is because angiotensin normally increases glomerular
capillary perfusion pressure, and so when ACE inhibitors reduce this
ability, with a background of already grossly reduced renal perfusion, the
glomerular filtration rate will fall. For this reason, the response to ACE
inhibitors should be monitored in patients with renal failure (and especially
so in patients with known peripheral arterial disease), and if renal function
worsens, various imaging techniques can be used to look for renal artery
stenosis (such as Doppler ultrasound and renal arteriography). Overall,
whilst ACE inhibitors should be avoided where possible in patients with
renal artery stenosis, they are beneficial in protecting the kidneys of renal
failure patients, and under specialist supervision can be started at a reduced
dose in patients with renal artery stenosis, especially if there is hypertension
that cannot be controlled by other means.
35. Microbiology
D. Gram-positive coccus
Staphylococcus aureus is a facultative anaerobe, i.e. it can survive without
31
using oxygen in its metabolism but will make use of it when available.
Gram-negative cocci include Neisseria gonorrhoea and Neisseria
meningitides. Gram-negative rods include Escherichia coli, Salmonella

species, Haemophilus influenzae, Pseudomonas aeruginosa, Enterobacter
species and Helicobacter pylori. Gram-positive rods include Clostridium
species and Listeria, whereas Gram-positive cocci of human significance
are either Staphylococci or Streptococci. Many Staphylococci are skin flora
in humans and commonly cause cellulitis and intravenous line and wound
infections. Initial appearance of bacteria upon Gram staining (positive
or negative, cocci or rods) can, together with the clinical picture, suggest
likely organisms and guide empirical antibiotic therapies before culture and
sensitivities have been performed.
Staphylococcus, from Greek staphyle = bunch of grapes (reference to the
clumping of cocci)
36. Skin lesions (1)

B. Basal cell carcinoma
The rolled edge, pearly appearance and telangiectasia are all classic features
of basal cell carcinoma. The history of sun exposure creates concerns of skin
cancer. It is not described as melanocytic, therefore malignant melanoma
seems highly unlikely (although amelanocytic malignant melanomas exist).
Squamous cell carcinomas are ill-defined keratotic nodules that often
ulcerate more so than basal cell carcinomas (BCCs). They can grow faster
than the slow growing BCCs. The risk factors are largely the same, however,
and the combined investigation and management of both is simple: excise
and send for histology (usually curative and diagnostic). Keratoacanthomas
are rapidly growing benign tumours that often mimic squamous cell
carcinomas. They can become quite large and typically develop a central
ulceration and necrosis pattern. They should be excised to exclude squamous
cell carcinoma as it is difficult to tell the two apart, although many resolve
spontaneously. Actinic keratoses are small erythematous silver-scaled
patches or papules that are common in sun damage, but are benign and can
be treated (if sufficiently large to warrant treatment) by cryotherapy, or if
diffuse can be treated by topical 5-fluorouracil cream or imiquimod cream
(to save repeated cryotherapy and associated minor scarring). They have the
potential to turn into squamous cell carcinomas after several years.
37. Diagnosis of abdominal pain (1)

A. Biliary colic
Biliary colic is a localised inflammation of the gallbladder due to gallstones.
The name in itself is a misnomer as the pain is rarely “colicky” in nature,
32
but more likely to be a severe and constant pain that may be related to the
ingestion of fatty foods. Gallstones typically present in patients with the

5 Fs – fat, forty, female, fair (Caucasian) and fertile (pre-menopausal).
Management is by removal of the gallbladder (cholecystectomy), usually
performed laparoscopically.
38. Ankylosing spondylitis

C. Pain present on waking in the early morning
AS is an inflammatory disorder of the back that is more common in males.
Patients present with lower back pain and stiffness of insidious onset that
is worse in the morning and gets better with exercise. There is poor spinal
flexion and in severe cases patients develop a rigid lower spine with a hunch
(known as the “question mark posture” or “hang dog posture”). AS may also
affect the large joints asymmetrically (although it affects the lumbar joints
symmetrically). AS is associated with a number of extra-articular features
that are remembered by the five As: Apical lung fibrosis, Anterior uveitis,
Achilles tendonitis/plantar fasciitis, Aortic regurgitation, and Amyloidosis.
This diagnosis of AS is made using Schober’s test: two fingers are placed
10 cm apart on the lower back of the patient (5 cm above and below the
L5 vertebra in the midline) and the patient is asked to flex. An increase
between the fingers of <5 cm indicates spinal stiffness. X-ray of the hip
shows blurred margins of the sacroiliac joints (sacroiliitis). Characteristic
radiological features of the spine in AS include erosion of the corners of
the vertebral bodies (Romanus lesions), the development of bony spurs
(syndesmophytes) and calcification of the spinal ligaments (bamboo spine).
Treatment options in AS are physiotherapy, exercise and slow-release non-
steroidal anti-inflammatory drugs (NSAIDs), e.g. indomethacin. Most
patients manage to lead a normal life, although severe cases may impair
ventilation.
AS is an example of a seronegative spondyloarthropathy – diseases associated
with HLA-B27 that are characterised by a lack of rheumatoid factor (hence
“seronegative”). Other spondyloarthropathies are psoriatic arthritis, Reiter
disease and enteropathic arthritis. The HLA-DR4 genotype is associated
with rheumatoid arthritis and type 1 diabetes mellitus, but not AS.
Ankylosing spondylitis originates from the Greek ankylos = bent
+ spondylos = vertebra
39. Mitral stenosis

C. Double impulse apex beat
Mitral stenosis occurs as a result of a chronic autoimmune attack upon the
mitral valves. This leads to scar tissue formation, which ultimately tethers
33
the leaflets and prevents them from opening fully. The autoimmune attack
Another random document with
no related content on Scribd:
tab. 118. follows Brisson, though everyone will be convinced that it
is a pigeon, at the very first examination of its bill. Mr. Edwards has
described and figured it, p. 269. t. 338. of the third volume of his
Gleanings. Its plumage is blue, or lead-coloured; the size, that of a
turkey. In that noble repository of natural history and learning, the
British Museum, there is a fine specimen of it. F.
120. They were found in a creek of the great isle, which forms this
bay; and which for that reason has been called Hammer Island, (Isle
aux Marteaux).
121. It is not known to what genus this plant belongs; a general,

but not systematical, description of it may be found in Mr. Valmont
de Bomare’s Dictionnaire d’ Histoire Naturelle, article Monbain. F.
122. M. de B. it seems can never sufficiently elevate the courage

and perseverance of his countrymen; on all occasions he praises
their disinterestedness, and endeavours to depreciate the merits of
the British sailors, by balancing their sufferings with the rewards
which an equitable government distributed to them. I have already
said something on this subject in a note to our author’s Introduction
(placed at the head of this work) and shall only add, that I should be
apt to suspect M. de B. to envy the British circumnavigators those
very rewards which he seems so much to despise, if I could combine
such base sentiments with his otherwise generous way of thinking.
F.
123. M. de Buffon has denied the existence of the Opossum or

Didelphis, Linn. in East India, though Piso, Valentyn, and Le Brun
have seen it in the Moluccas and in Java: M. de Buffon’s own
countryman, M. de Bougainville, now likewise asserts their being
upon Boero, in a manner so little equivocal, that there can be no
doubt of the Opossum genus inhabiting the East Indies, though the
particular species is unknown. F.
124. This is the great Bat of Ternate, Penn. Syn. Quad. p. 359.
and Linnæus’s Vespertilio Vampyrus. F.
125. Sous-Marchand.
126. Galere tentée: we suppose M. de Bougainville means a

galley, with her awnings spread. F.
127. Of six feet French measure each.
128. The word Sultan is not of Arabic, but of Tartarian origin; but
early introduced into the Arabian language by the Turks that were in
the service of the Caliphs. F.
129. This name is wretchedly disfigured from the Dutch, Schout-

by-Nacht, which signifies Rear Admiral. F.
130. Salawati. F.
131. Lord Sandwich’s son never was in any of these expeditions; it

therefore is evident, that M. de Bougainville has been misinformed in
regard to this particular. F.
132. Mr. Dalrymple never was at Batavia, nor Bencoolen; he left

China in January 1765, and arrived in England in July 1765, since
when he has never been out of the kingdom. From whence it must
be obvious, M. de Bougainville is entirely mistaken in what he says
concerning M. Dalrymple.
133. Diego Rays. F.
134. Equal to our midshipman. F.
135. We are very ready to do justice to Mr. Bougainville, when he

presents us with a new and interesting observation; but when he,
without the least necessity, becomes the advocate of tyranny and
oppression, we cannot let these sentiments pass unnoticed. It would
have appeared to us impossible, that such an idea as this could
enter into any man’s head who is in his right senses: he wrote down
this strange assertion, either being carried away by the itch to say
something extraordinary and paradoxical, or in order to make slavery
more tolerable to his fellow Frenchmen—Slavery endeavours to
extirpate and to smother all sentiments of honour, which only can
operate in the breast of a really free man; true honour, therefore,
and slavery, are in direct opposition, and can be combined as little as
fire and water. If Mr. B. threw this sentence out, in order to alleviate
the yoke of tyranny his country groans under, we think we could
excuse it in some measure, as he would then act from principles of
humanity. But if the irresistible desire of saying something new was
the prevalent motive with him, it has much the appearance as if he
were willing to insult the poor victims of despotism. The generous
and amiable character which M. B. from other instances appears in,
prompts us to wish, that this sentence had been omitted by him. F.
136. I must here observe, that I have not altered the spelling of
the words at all; and the reader will therefore take notice, that they
should be pronounced according to the rules of the French language.
F.
Transcriber’s Note
The Taitian Vocabulary at the end of the text was
printed in two columns, which are presented here as a
single continuous table, interspersed with notes.
Given the age of the text, any corrections to spelling is
problematic. Corrections have only been made when
there are ample examples of our modern spelling.
In the quotation from Virgil at the opening of Part II
on p. 199, the English word ‘and’ was (no doubt)
mistakenly used rather than the Latin ‘et’. It is given
correctly in the French original.
The name of the marquis de Buccarelli (appearing as
such ten times) is given three times (pp. 113-117) as
‘Bucarelli’. These have been corrected to facilitate text
searches.
On p. 429, the translation is missing the word ‘time’,
which has been established based on the French original.
See below.
Errors deemed most likely to be the printer’s have
been corrected, and are noted here. The references are
to the page and line in the original.
10.5 the varia[tia]tions N. which Removed.
we met with.
14.18 is insuf[fi]cient to encourage Inserted.
43.25 the wars of king Will[i]am> Inserted.
46.12 The map w[h]ich> we give Inserted.
91.6 Navigation from Inserted.
Montevid[e]o to Baragan.
92.17 goes to be repa[ri/ired there Transposed.
98.11 upon this [carrier/career] Mistranslation.
113.17 the marquis de Buc[c]arelli Inserted.
113.22 upon the Ur[a/u]guay Replaced.
115.6 the marquis de Buc[c]arelli Inserted.
117.7 Don Francisco Buc[c]arelli y Inserted.
Ursua
135.25 to a[ ]void the rocks Removed.
155.20 to go in my pinna[n]ce Removed.
173.22 Two other p[a/e]riaguas Replaced.
followed
179.1 and mistrust amongst Replaced.
them[,/.]
180.2 our chaplain administ[e]red Inserted.
190.10 bears E. 9[°] N. and W. 9° S. Restored.
199.9 errantes terris [and/et] Replaced.
fluctibus æstas
199.18 make good Completed.
astronomi[-/ical]observations
201.25 Mr. Bou[n]gainville writes Removed.
207.19 as the inhabi[bi]tants of the Removed.
first island
235.16 [w/W]e then weighed the Replaced.
stream-anchor
272.7 is soft, harmoni[o]us, and Inserted.
easy
293.14 extended on the south[.] Removed.
side
317.22 to assist us in stem[m]ing Inserted.
the tide
358.20 The currents ceased Inserted.
set[t]ing us
386.8 the isle of Pang[e/a]sani Replaced.
429.2 very little at a [time] from Added.
each person
437.8 to get to the anchor[a]ge Inserted.
449.2 the isles of Amsterdam and Transposed.
Midd[le/le]burg
463.22 I[s/t] is not without reason Replaced.
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Get Ahead Medicine 300 Sbas For Finals 1St Edition Benjamin Mcneillis

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Introduction to Get Ahead Medicine xiv

Practice Practice Paper 1: Questions 1

Practice Paper 1: Answers 16

Practice Paper 2: Questions 40

Practice Paper 2: Answers 57

Practice Paper 3: Questions 82

Practice Paper 3: Answers 99

Practice Paper 4: Questions 124

1. Alzheimer’s disease 164

Practice Paper 5: Answers 181

Practice Paper 6: Questions 203

Practice Paper 6: Answers 219

Index of topics covered 243

HOW TO PASS YOUR EXAMS

DURING THE EXAM

Introduction to Get Ahead Medicine

2. Obstructive renal impairment

3. Management of skin lesions (1)

A 68-year-old man who is recently diagnosed with lung cancer is admitted

6. Chronic obstructive pulmonary disease

7. Management of asthma (1)

Practice Paper 1: Questions

9. Eczema versus psoriasis

10. Diagnosis of multiple sclerosis (1)

A 67-year-old man is discharged from hospital following an incision and

12. Diagnosis of chest pain (1)

13. Risk factors for ischaemic heart disease

14. Diagnosis of cough (1)

Practice Paper 1: Questions

15. Diagnosis of vertigo

Following a protracted stay in hospital following a severe chest infection,

18. Diagnosis of malaria

19. Electrocardiogram (1)

20. Investigation of deranged liver function tests

Practice Paper 1: Questions

21. Epigastric pain (1)

22. Gout prophylaxis

Which of the following conditions is associated with sclerosing cholangitis?

25. Investigation of status epilepticus

26. Shortness of breath (1)

27. Aortic regurgitation

Practice Paper 1: Questions

28. Management of oliguria (1)

An 83-year-old man who was diagnosed as having Parkinson’s disease 3

32. Coronary circulation